Analysis of the correlations of hypertension complicated with or without hypertensive nephropathy with glucose and lipid metabolism, vascular endothelial function, inflammation, oxidative stress and course of disease

Zhang, Wei; Lü, Qing; Sheng, Yong; Sun, Xu; Chen, Xiaoping

doi:10.23736/s0031-0808.19.03649-8

Cited by 3 publications

(2 citation statements)

References 4 publications

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“…In addition, it has reported that AMPK activation promotes the entry of nuclear factor erythroid 2-related factor-2 (Nrf2) into the nucleus, up-regulates the expressions of antioxidant factors such as heme oxygenase-1 (HO-1) and NAD (P) H:quinone oxidoreductase (NQO-1), thus exerting the effect of antioxidant stress (Ni et al 2019 ; Yamakage et al 2020 ). Notably, the injury of renal tubular epithelial cells induced by releasing of inflammatory mediators and oxidative stress plays a key role in the pathogenesis of hypertensive nephropathy (Ding et al 2019 ; Zhang et al 2020 ). Moreover, a study shown that FGF21 prevented type 2 diabetic-induced cardiomyopathy through activation of AMPK-mediated antioxidation and lipid-lowering effects (Yang et al 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism

Weng

et al. 2021

Mol Med

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Background Patients with salt-sensitive hypertension are often accompanied with severe renal damage and accelerate to end-stage renal disease, which currently lacks effective treatment. Fibroblast growth factor 21 (FGF21) has been shown to suppress nephropathy in both type 1 and type 2 diabetes mice. Here, we aimed to investigate the therapeutic effect of FGF21 in salt-sensitive hypertension-induced nephropathy. Methods Changes of FGF21 expression in deoxycorticosterone acetate (DOCA)-salt-induced hypertensive mice were detected. The influence of FGF21 knockout in mice on DOCA-salt-induced nephropathy were determined. Recombinant human FGF21 (rhFGF21) was intraperitoneally injected into DOCA-salt-induced nephropathy mice, and then the inflammatory factors, oxidative stress levels and kidney injury-related indicators were observed. In vitro, human renal tubular epithelial cells (HK-2) were challenged by palmitate acid (PA) with or without FGF21, and then changes in inflammation and oxidative stress indicators were tested. Results We observed significant elevation in circulating levels and renal expression of FGF21 in DOCA-salt-induced hypertensive mice. We found that deletion of FGF21 in mice aggravated DOCA-salt-induced nephropathy. Supplementation with rhFGF21 reversed DOCA-salt-induced kidney injury. Mechanically, rhFGF21 induced AMPK activation in DOCA-salt-treated mice and PA-stimulated HK-2 cells, which inhibited NF-κB-regulated inflammation and Nrf2-mediated oxidative stress and thus, is important for rhFGF21 protection against DOCA-salt-induced nephropathy. Conclusion These findings indicated that rhFGF21 could be a promising pharmacological strategy for the treatment of salt-sensitive hypertension-induced nephropathy.

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Section: Introductionmentioning

confidence: 99%

Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism

Weng

et al. 2021

Mol Med

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show abstract

“…In addition, it has reported that AMPK activation promotes the entry of nuclear factor erythroid 2-related factor-2 (Nrf2) into the nucleus, up-regulates the expressions of antioxidant factors such as heme oxygenase-1 (HO-1) and NAD (P) H:quinone oxidoreductase (NQO-1), thus exerting the effect of antioxidant stress (Ni, Shen et al, 2019;Yamakage, Tanaka et al, 2020). Notably, the injury of renal tubular epithelial cells induced by releasing of in ammatory mediators and oxidative stress plays a key role in the pathogenesis of hypertensive nephropathy (Ding, Zhou et al, 2019;Zhang, Cheng et al, 2020). Moreover, a study shown that FGF21 prevented type 2 diabetic-induced cardiomyopathy through activation of AMPK-mediated antioxidation and lipid-lowering effects (Yang, Feng et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Fibroblast Growth Factor 21 Attenuates Salt-sensitive Hypertension-induced Nephropathy Through Anti-inflammation and Anti-oxidation Mechanism

Weng

et al. 2021

Preprint

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BackgroundPatients with salt-sensitive hypertension are often accompanied with severe renal damage and accelerate to end-stage renal disease, which currently lacks effective treatment. Fibroblast growth factor 21 (FGF21) has been shown to suppress nephropathy in both type 1 and type 2 diabetes mice. Here, we aimed to investigate the therapeutic effect of FGF21 in salt-sensitive hypertension-induced nephropathy.MethodsChanges of FGF21 expression in deoxycorticosterone acetate (DOCA)-salt-induced hypertensive mice were detected. The influence of FGF21 knockout in mice on DOCA-salt-induced nephropathy were determined. Recombinant human FGF21 (rhFGF21) was intraperitoneally injected into DOCA-salt-induced nephropathy mice, and then the inflammatory factors, oxidative stress levels and kidney injury-related indicators were observed. In vitro, human renal tubular epithelial cells (HK-2) were challenged by palmitate acid (PA) with or without FGF21, and then changes in inflammation and oxidative stress indicators were tested.ResultsWe observed significant elevation in circulating levels and renal expression of FGF21 in DOCA-salt-induced hypertensive mice. We found that deletion of FGF21 in mice aggravated DOCA-salt-induced nephropathy. Supplementation with rhFGF21 reversed DOCA-salt-induced kidney injury. Mechanically, rhFGF21 induced AMPK activation in DOCA-salt-treated mice and PA-stimulated HK-2 cells, which inhibited NF-κB-regulated inflammation and Nrf2-mediated oxidative stress and thus, is important for rhFGF21 protection against DOCA-salt-induced nephropathy. ConclusionThese findings indicated that rhFGF21 could be a promising pharmacological strategy for the treatment of salt-sensitive hypertension-induced nephropathy.

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Roles of SIRT6 in kidney disease: a novel therapeutic target

Yang

Feng

Liang

et al. 2021

Cell. Mol. Life Sci.

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Analysis of the correlations of hypertension complicated with or without hypertensive nephropathy with glucose and lipid metabolism, vascular endothelial function, inflammation, oxidative stress and course of disease

Cited by 3 publications

References 4 publications

Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism

Fibroblast growth factor 21 attenuates salt-sensitive hypertension-induced nephropathy through anti-inflammation and anti-oxidation mechanism

Fibroblast Growth Factor 21 Attenuates Salt-sensitive Hypertension-induced Nephropathy Through Anti-inflammation and Anti-oxidation Mechanism

Roles of SIRT6 in kidney disease: a novel therapeutic target

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